Vore, A. P., Chang, E. H., Hoppe, J. E., Butler, M. G., Forrester, S., Schneider, M. C., Smith, L. L., Burke, D. W., Campbell, C. A., & Smith, R. J. (2005). Deletion of and novel missense mutation in POU3F4 in 2 families segregating X-linked nonsyndromic deafness. Archives of otolaryngology--head & neck surgery, 131(12), 1057-63.
To analyze the physical manifestations and genetic features of 2 families segregating X-linked deafness, which is most commonly reported to be caused by mutations of the POU domain gene POU3F4 at the DFN3 locus.
Barry, J. Y., McCrary, H. C., Kent, S., Saleh, A. A., Chang, E. H., & Chiu, A. G. (2016). The Triple Aim and its implications on the management of chronic rhinosinusitis. American journal of rhinology & allergy, 30(5), 344-50.
Accountable care organizations (ACO) and alternative payment models are a sign of the change in reimbursement from fee-for-service to value-based reimbursement. The focus of health care under ACOs is represented by the Triple Aim: to improve the experience of health care, improve the health of populations, and reduce the per capita costs. Individuals with chronic rhinosinusitis (CRS) are heavy consumers of health care services. Results of recent studies have indicated that there is the potential for improved outcomes and cost savings from early surgical intervention. Adhering to the principles of the Triple Aim may signal a paradigm shift in regard to timing of intervention for CRS in certain patients.
Husein, M., Chang, E., Cable, B., Karnell, M., Karnell, L. H., & Canady, J. W. (2004). Outcomes for children with submucous cleft palate and velopharyngeal insufficiency. The Journal of otolaryngology, 33(4), 222-6.
To review the outcomes of children with submucous cleft palate who also have velopharyngeal insufficiency (VPI).
Stoltz, D. A., Meyerholz, D. K., Pezzulo, A. A., Ramachandran, S., Rogan, M. P., Davis, G. J., Hanfland, R. A., Wohlford-Lenane, C., Dohrn, C. L., Bartlett, J. A., Nelson, G. A., Chang, E. H., Taft, P. J., Ludwig, P. S., Estin, M., Hornick, E. E., Launspach, J. L., Samuel, M., Rokhlina, T., , Karp, P. H., et al. (2010). Cystic fibrosis pigs develop lung disease and exhibit defective bacterial eradication at birth. Science translational medicine, 2(29), 29ra31.
Lung disease causes most of the morbidity and mortality in cystic fibrosis (CF). Understanding the pathogenesis of this disease has been hindered, however, by the lack of an animal model with characteristic features of CF. To overcome this problem, we recently generated pigs with mutated CFTR genes. We now report that, within months of birth, CF pigs spontaneously developed hallmark features of CF lung disease, including airway inflammation, remodeling, mucus accumulation, and infection. Their lungs contained multiple bacterial species, suggesting that the lungs of CF pigs have a host defense defect against a wide spectrum of bacteria. In humans, the temporal and causal relations between inflammation and infection have remained uncertain. To investigate these processes, we studied newborn pigs. Their lungs showed no inflammation but were less often sterile than controls. Moreover, after introduction of bacteria into their lungs, pigs with CF failed to eradicate bacteria as effectively as wild-type pigs. These results suggest that impaired bacterial elimination is the pathogenic event that initiates a cascade of inflammation and pathology in CF lungs. Our finding that pigs with CF have a host defense defect against bacteria within hours of birth provides an opportunity to further investigate CF pathogenesis and to test therapeutic and preventive strategies that could be deployed before secondary consequences develop.
Willis, A. L., Calton, J. B., Carr, T. F., Chiu, A. G., & Chang, E. H. (2016). Differentiating live from dead: a novel profile of the sinus microbiome.. American Journal of Rhinology and Allergy.
